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肾缺血后大鼠脑线粒体呼吸链的抑制可被 N-乙酰半胱氨酸和去铁胺所预防。

Inhibition of mitochondrial respiratory chain in the brain of rats after renal ischemia is prevented by N-acetylcysteine and deferoxamine.

机构信息

Unidade Acadêmica de Ciências da Saúde, Universidade do Extremo Sul Catarinense, Criciúma, SC, Brazil.

出版信息

Metab Brain Dis. 2010 Jun;25(2):219-25. doi: 10.1007/s11011-010-9187-9. Epub 2010 Apr 28.

DOI:10.1007/s11011-010-9187-9
PMID:20424907
Abstract

We evaluated the activities of mitochondrial respiratory chain complexes in the brain of rats after renal ischemia and the effect of administration of the antioxidants N-acetylcysteine (NAC) and deferoxamine (DFX). The rats were divided into the groups: sham (control) or renal ischemia treated with saline, NAC 20 mg/kg, DFX 20 mg/kg or both antioxidants. Complex I activity was inhibited in hippocampus, striatum, prefrontal cortex and cerebral cortex of rats 1 and 6 h after renal ischemia and that the treatment with a combination of NAC and DFX prevented such effect. Complex I activity was not altered in hippocampus, striatum, prefrontal cortex and cerebral cortex of rats 12 h after renal ischemia. Complexes II and III activities were not altered in hippocampus, striatum, prefrontal cortex and cerebral cortex of rats 1, 6 and 12 h after renal ischemia. Complex IV activity was inhibited in hippocampus, striatum, prefrontal cortex and cerebral cortex of rats 1 h after renal ischemia, but the treatment with the combination of NAC and DFX was able to prevent this inhibition. Complex IV activity was not altered in hippocampus, striatum, prefrontal cortex and cerebral cortex of rats 6 and 12 h after renal ischemia. These results suggest that the inhibition of mitochondrial respiratory chain after renal ischemia might play a role in the pathogenesis of uremic encephalopathy.

摘要

我们评估了肾缺血后大鼠大脑中线粒体呼吸链复合物的活性以及抗氧化剂 N-乙酰半胱氨酸 (NAC) 和去铁胺 (DFX) 给药的影响。将大鼠分为以下几组:假手术(对照)或用生理盐水、NAC 20mg/kg、DFX 20mg/kg 或两种抗氧化剂处理的肾缺血。肾缺血 1 和 6 小时后,大鼠海马体、纹状体、前额叶皮质和大脑皮质的复合物 I 活性受到抑制,而联合使用 NAC 和 DFX 可预防这种作用。肾缺血 12 小时后,大鼠海马体、纹状体、前额叶皮质和大脑皮质的复合物 I 活性未改变。肾缺血 1、6 和 12 小时后,大鼠海马体、纹状体、前额叶皮质和大脑皮质的复合物 II 和 III 活性未改变。肾缺血 1 小时后,大鼠海马体、纹状体、前额叶皮质和大脑皮质的复合物 IV 活性受到抑制,但联合使用 NAC 和 DFX 可预防这种抑制。肾缺血 6 和 12 小时后,大鼠海马体、纹状体、前额叶皮质和大脑皮质的复合物 IV 活性未改变。这些结果表明,肾缺血后线粒体呼吸链的抑制可能在尿毒症脑病的发病机制中起作用。

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本文引用的文献

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Inhibition of brain creatine kinase activity after renal ischemia is attenuated by N-acetylcysteine and deferoxamine administration.肾缺血后,N-乙酰半胱氨酸和去铁胺给药可减轻脑肌酸激酶活性的抑制。
Neurosci Lett. 2008 Mar 21;434(1):139-43. doi: 10.1016/j.neulet.2008.01.051. Epub 2008 Jan 31.
2
Brain creatine kinase activity in an animal model of mania.躁狂症动物模型中的脑肌酸激酶活性
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Chronic renal failure-induced multiple-organ injury in rats is alleviated by the selective CysLT1 receptor antagonist montelukast.
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Metab Brain Dis. 2017 Apr;32(2):557-564. doi: 10.1007/s11011-016-9936-5. Epub 2016 Dec 6.
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Evaluation of brain and kidney energy metabolism in an animal model of contrast-induced nephropathy.评价造影剂肾病动物模型的脑和肾能量代谢。
Metab Brain Dis. 2011 Jun;26(2):115-22. doi: 10.1007/s11011-011-9240-3. Epub 2011 Mar 25.
选择性半胱氨酰白三烯1(CysLT1)受体拮抗剂孟鲁司特可减轻大鼠慢性肾衰竭诱导的多器官损伤。
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